T Nakagawa

Summary

Affiliation: University of Florida
Country: USA

Publications

  1. ncbi A breakthrough in diabetic nephropathy: the role of endothelial dysfunction
    Takahiko Nakagawa
    Division of Nephrology, Hypertension and Transplantation, University of Florida, PO Box 100224, Gainesville, FL 32610-0224, USA
    Nephrol Dial Transplant 22:2775-7. 2007
  2. ncbi TGF-beta induces proangiogenic and antiangiogenic factors via parallel but distinct Smad pathways
    Takahiko Nakagawa
    Division of Nephrology Medicine, Baylor College of Medicine, Houston, Texas, USA
    Kidney Int 66:605-13. 2004
  3. ncbi Uncoupling of VEGF with NO as a mechanism for diabetic nephropathy
    Takahiko Nakagawa
    Division of Nephrology, Hypertension and Transplantation, University of Florida, PO Box 100224, Gainesville, FL 32610 0224, USA
    Diabetes Res Clin Pract 82:S67-9. 2008
  4. ncbi Role of ERK1/2 and p38 mitogen-activated protein kinases in the regulation of thrombospondin-1 by TGF-beta1 in rat proximal tubular cells and mouse fibroblasts
    Takahiko Nakagawa
    Division of Nephrology, Hypertension and Transplantation, University of Florida, P O Box 100224, Gainesville, FL 32610 0224, USA
    J Am Soc Nephrol 16:899-904. 2005
  5. ncbi A causal role for uric acid in fructose-induced metabolic syndrome
    Takahiko Nakagawa
    Division of Nephrology, Hypertension, and Transplantation, PO Box 100224, University of Florida, Gainesville, FL 32610, USA
    Am J Physiol Renal Physiol 290:F625-31. 2006
  6. ncbi The conundrum of hyperuricemia, metabolic syndrome, and renal disease
    Takahiko Nakagawa
    Division of Nephrology, Hypertension and Transplantation, University of Florida, PO Box 100224, Gainesville, FL, 32610, USA
    Intern Emerg Med 3:313-8. 2008
  7. ncbi Uric acid--a uremic toxin?
    Takahiko Nakagawa
    Division of Nephrology, Hypertension and Transplantation, University of Florida, Gainesville, FL 32610 0224, USA
    Blood Purif 24:67-70. 2006
  8. ncbi Uncoupling of vascular endothelial growth factor with nitric oxide as a mechanism for diabetic vasculopathy
    Takahiko Nakagawa
    Division of Nephrology, Hypertension and Transplantation, University of Florida, PO Box 100224, Gainesville, FL 32610, USA
    J Am Soc Nephrol 17:736-45. 2006
  9. ncbi Unearthing uric acid: an ancient factor with recently found significance in renal and cardiovascular disease
    T Nakagawa
    Division of Nephrology, Hypertension, and Renal Transplantation, University of Florida, Gainesville, 32610, USA
    Kidney Int 69:1722-5. 2006
  10. ncbi Hypothesis: fructose-induced hyperuricemia as a causal mechanism for the epidemic of the metabolic syndrome
    Takahiko Nakagawa
    Division of Nephrology, Hypertension, and Transplantation, University of Florida, Gainesville, FL 32610, USA
    Nat Clin Pract Nephrol 1:80-6. 2005

Detail Information

Publications66

  1. ncbi A breakthrough in diabetic nephropathy: the role of endothelial dysfunction
    Takahiko Nakagawa
    Division of Nephrology, Hypertension and Transplantation, University of Florida, PO Box 100224, Gainesville, FL 32610-0224, USA
    Nephrol Dial Transplant 22:2775-7. 2007
  2. ncbi TGF-beta induces proangiogenic and antiangiogenic factors via parallel but distinct Smad pathways
    Takahiko Nakagawa
    Division of Nephrology Medicine, Baylor College of Medicine, Houston, Texas, USA
    Kidney Int 66:605-13. 2004
    ..Recent studies have shown that VEGF-A as well as TSP-1 is regulated by transforming growth factor-beta1 (TGF-beta1), but the mechanism remains unclear...
  3. ncbi Uncoupling of VEGF with NO as a mechanism for diabetic nephropathy
    Takahiko Nakagawa
    Division of Nephrology, Hypertension and Transplantation, University of Florida, PO Box 100224, Gainesville, FL 32610 0224, USA
    Diabetes Res Clin Pract 82:S67-9. 2008
    ....
  4. ncbi Role of ERK1/2 and p38 mitogen-activated protein kinases in the regulation of thrombospondin-1 by TGF-beta1 in rat proximal tubular cells and mouse fibroblasts
    Takahiko Nakagawa
    Division of Nephrology, Hypertension and Transplantation, University of Florida, P O Box 100224, Gainesville, FL 32610 0224, USA
    J Am Soc Nephrol 16:899-904. 2005
    ..Because TSP-1 is a major antiangiogenic molecule and an activator of TGF-beta1, this provides an important insight to the mechanism by which TGF-beta1 may mediate interstitial fibrosis and progressive renal disease...
  5. ncbi A causal role for uric acid in fructose-induced metabolic syndrome
    Takahiko Nakagawa
    Division of Nephrology, Hypertension, and Transplantation, PO Box 100224, University of Florida, Gainesville, FL 32610, USA
    Am J Physiol Renal Physiol 290:F625-31. 2006
    ..Fructose may have a major role in the epidemic of metabolic syndrome and obesity due to its ability to raise uric acid...
  6. ncbi The conundrum of hyperuricemia, metabolic syndrome, and renal disease
    Takahiko Nakagawa
    Division of Nephrology, Hypertension and Transplantation, University of Florida, PO Box 100224, Gainesville, FL, 32610, USA
    Intern Emerg Med 3:313-8. 2008
    ..In this review, we discuss the clinical and experimental evidence for a causal role of hyperuricemia in renal diseases and potential relationships of hyperuricemia with metabolic syndrome...
  7. ncbi Uric acid--a uremic toxin?
    Takahiko Nakagawa
    Division of Nephrology, Hypertension and Transplantation, University of Florida, Gainesville, FL 32610 0224, USA
    Blood Purif 24:67-70. 2006
    ..In progressive renal disease, such as cyclosporine nephropathy and remnant kidney in rat, uric acid accelerated the progression of renal disease. Thus, we concluded that uric acid is not a simple marker, but a cause of renal disease...
  8. ncbi Uncoupling of vascular endothelial growth factor with nitric oxide as a mechanism for diabetic vasculopathy
    Takahiko Nakagawa
    Division of Nephrology, Hypertension and Transplantation, University of Florida, PO Box 100224, Gainesville, FL 32610, USA
    J Am Soc Nephrol 17:736-45. 2006
    ..These results may provide new insights into the understanding of the mechanism of diabetic vascular disease...
  9. ncbi Unearthing uric acid: an ancient factor with recently found significance in renal and cardiovascular disease
    T Nakagawa
    Division of Nephrology, Hypertension, and Renal Transplantation, University of Florida, Gainesville, 32610, USA
    Kidney Int 69:1722-5. 2006
    ..Clinical studies are urgently needed to examine this important possibility...
  10. ncbi Hypothesis: fructose-induced hyperuricemia as a causal mechanism for the epidemic of the metabolic syndrome
    Takahiko Nakagawa
    Division of Nephrology, Hypertension, and Transplantation, University of Florida, Gainesville, FL 32610, USA
    Nat Clin Pract Nephrol 1:80-6. 2005
    ..Studies in humans should be performed to address whether lowering uric acid levels will help to prevent this condition...
  11. ncbi Diabetic endothelial nitric oxide synthase knockout mice develop advanced diabetic nephropathy
    Takahiko Nakagawa
    Division of Nephrology, Hypertension and Transplantation, University of Florida, PO Box 100224, Gainesville, FL 32610 0224, USA
    J Am Soc Nephrol 18:539-50. 2007
    ..It was postulated that endothelial dysfunction should predict nephropathy and that correction of the dysfunction may prevent these important complications...
  12. ncbi Uncoupling of the VEGF-endothelial nitric oxide axis in diabetic nephropathy: an explanation for the paradoxical effects of VEGF in renal disease
    Takahiko Nakagawa
    Division of Nephrology, Hypertension, and Transplantation, University of Florida, PO Box 100224, Gainesville, FL 32610 0224, USA
    Am J Physiol Renal Physiol 292:F1665-72. 2007
    ....
  13. ncbi Differential regulation of VEGF by TGF-beta and hypoxia in rat proximal tubular cells
    Takahiko Nakagawa
    Division of Nephrology, Hypertension, and Transplantation, University of Florida, Gainesville, FL 32610 0224, USA
    Am J Physiol Renal Physiol 287:F658-64. 2004
    ..Thus TGF-beta and hypoxia act via additive/synergistic but distinct pathways to stimulate VEGF in proximal tubular cells, a finding that may be important in understanding how VEGF is stimulated in renal disease...
  14. ncbi Thiazide diuretics exacerbate fructose-induced metabolic syndrome
    Sirirat Reungjui
    Division of Nephrology, Hypertension and Transplantation, University of Florida, Gainesville, Florida, USA
    J Am Soc Nephrol 18:2724-31. 2007
    ..Addition of potassium supplements and allopurinol with thiazides might be helpful in the management of metabolic syndrome...
  15. ncbi A role for uric acid in the progression of renal disease
    Duk Hee Kang
    Division of Nephrology, Baylor College of Medicine, Houston, Texas, USA
    J Am Soc Nephrol 13:2888-97. 2002
    ..These studies provide direct evidence that uric acid may be a true mediator of renal disease and progression...
  16. ncbi Effect of lowering uric acid on renal disease in the type 2 diabetic db/db mice
    Tomoki Kosugi
    Division of Nephrology, University of Florida, Gainesville, Florida, USA
    Am J Physiol Renal Physiol 297:F481-8. 2009
    ..In conclusion, hyperuricemia has a pathogenic role in the mild tubulointerstitial injury associated with diabetic nephropathy but not glomerular damage in db/db mice. Lowering uric acid may reduce tubulointerstitial injury in diabetes...
  17. ncbi Lowering blood pressure blocks mesangiolysis and mesangial nodules, but not tubulointerstitial injury, in diabetic eNOS knockout mice
    Tomoki Kosugi
    Division of Nephrology, University of Florida, Gainesville, Florida, USA
    Am J Pathol 174:1221-9. 2009
    ..This study could provide insights into the pathogenesis of advanced diabetic nephropathy in the presence of endothelial dysfunction...
  18. ncbi Nitric oxide modulates vascular disease in the remnant kidney model
    Duk Hee Kang
    Division of Nephrology, Baylor College of Medicine, Houston, Texas, USA
    Am J Pathol 161:239-48. 2002
    ..Interestingly, inhibition of NO synthesis did not lead to a loss of the preglomerular endothelium, which may relate to the effect of NO blockade to stimulate VEGF synthesis in the adjacent vascular smooth muscle cell...
  19. ncbi Lead, at low levels, accelerates arteriolopathy and tubulointerstitial injury in chronic kidney disease
    Carlos Roncal
    Division of Nephrology, Hypertension, and Transplantation, University of Florida, Gainesville, FL 32610 0224, USA
    Am J Physiol Renal Physiol 293:F1391-6. 2007
    ..In conclusion, lead accelerates chronic renal disease, primarily by raising blood pressure and accelerating microvascular and tubulointerstitial injury...
  20. ncbi Uric acid, hominoid evolution, and the pathogenesis of salt-sensitivity
    Susumu Watanabe
    Division of Nephrology, Baylor College of Medicine, Houston, Tex 77030, USA
    Hypertension 40:355-60. 2002
    ..Although it provided a survival advantage to early hominoids, hyperuricemia may have a major role in the current cardiovascular disease epidemic...
  21. ncbi Dietary fructose causes tubulointerstitial injury in the normal rat kidney
    Takahiro Nakayama
    Division of Nephrology, University of Florida, Gainesville, Florida, USA
    Am J Physiol Renal Physiol 298:F712-20. 2010
    ..The effect is independent of total energy intake and is associated with focal tubulointerstitial injury. These studies may provide a mechanism by which metabolic syndrome causes renal disease...
  22. ncbi Uric acid stimulates monocyte chemoattractant protein-1 production in vascular smooth muscle cells via mitogen-activated protein kinase and cyclooxygenase-2
    John Kanellis
    Division of Nephrology, Baylor College of Medicine, SM 1273, 6550 Fannin St, Houston TX 77030
    Hypertension 41:1287-93. 2003
    ..Uric acid regulates critical proinflammatory pathways in VSMCs, suggesting it may have a role in the vascular changes associated with hypertension and vascular disease...
  23. ncbi The pivotal role of VEGF on glomerular macrophage infiltration in advanced diabetic nephropathy
    Waichi Sato
    Division of Nephrology, Department of Medicine, University of Florida, Gainesville, FL 32610 0224, USA
    Lab Invest 88:949-61. 2008
    ..In summary, NO negatively regulates VEGF-induced macrophage migration by inhibiting Flt-1 expression. The VEGF-endothelial NO uncoupling pathway might partially explain how VEGF causes glomerular disease in diabetes...
  24. ncbi Inhibition of p38 mitogen-activated protein kinase augments progression of remnant kidney model by activating the ERK pathway
    Ryuji Ohashi
    Division of Nephrology, Baylor College of Medicine, Houston Texas 77030, USA
    Am J Pathol 164:477-85. 2004
    ..We conclude that blocking p38-dependent inflammation may have resulted in enhanced proliferation and increased ERK1/2 activation, and thereby explains the worse renal lesions observed...
  25. ncbi Endothelial injury due to eNOS deficiency accelerates the progression of chronic renal disease in the mouse
    Takahiro Nakayama
    Division of Nephrology, Univ of Colorado Denver, P O Box C281, Aurora, CO 80045, USA
    Am J Physiol Renal Physiol 296:F317-27. 2009
    ..A lack of eNOS accelerates both glomerular and tubulointerstitial injury with a loss of glomerular capillaries and peritubular capillaries. Impaired endothelial function is likely a direct risk factor for renal disease...
  26. ncbi Angiostatin overexpression is associated with an improvement in chronic kidney injury by an anti-inflammatory mechanism
    Wei Mu
    Division of Nephrology, University of Florida, Gainesville, FL, USA
    Am J Physiol Renal Physiol 296:F145-52. 2009
    ..However, its anti-angiogenic actions suggest countering effects that could partially offset its benefit in chronic kidney diseases...
  27. ncbi Hyperuricemia induces a primary renal arteriolopathy in rats by a blood pressure-independent mechanism
    Marilda Mazzali
    Division of Nephrology, Baylor College of Medicine, Houston, Texas 77030, USA
    Am J Physiol Renal Physiol 282:F991-7. 2002
    ..Thus hyperuricemia induces a renal arteriolopathy in rats that is blood pressure independent and involves the renin-angiotensin system...
  28. ncbi eNOS knockout mice with advanced diabetic nephropathy have less benefit from renin-angiotensin blockade than from aldosterone receptor antagonists
    Tomoki Kosugi
    Division of Nephrology, University of Florida, Gainesville, Florida, USA
    Am J Pathol 176:619-29. 2010
    ..In conclusion, an impaired endothelial NO response could lessen the benefit of RAS inhibition in diabetic renal disease. Aldosterone blockade may provide superior protection in this setting...
  29. ncbi A single pathway for the development of essential hypertension
    John Kanellis
    Division of Nephrology, Baylor College of Medicine, Houston, Texas 77030, USA
    Cardiol Rev 11:180-96. 2003
  30. ncbi Serum uric acid: a risk factor and a target for treatment?
    Daniel I Feig
    Department of Pediatrics, Renal Section, Baylor College of Medicine, Houston, TX 77030, USA
    J Am Soc Nephrol 17:S69-73. 2006
    ..Although the investigations are still preliminary, serum uric acid represents a possible new and intriguing target for the reduction of morbidity and mortality associated with hypertension and CV disease...
  31. ncbi Comparison of free fructose and glucose to sucrose in the ability to cause fatty liver
    Laura G Sanchez-Lozada
    Division of Nephrology, Hypertension and Transplantation, University of Florida, Gainesville, FL, USA
    Eur J Nutr 49:1-9. 2010
    ....
  32. ncbi Soluble Flt-1 gene therapy ameliorates albuminuria but accelerates tubulointerstitial injury in diabetic mice
    Tomoki Kosugi
    Division of Nephrology, University of Florida, Gainesville, Florida, USA
    Am J Physiol Renal Physiol 298:F609-16. 2010
    ..These data suggest systemic overexpression of sFlt-1 will not likely be useful for treating diabetic nephropathy...
  33. ncbi Pathogenesis of essential hypertension: historical paradigms and modern insights
    Richard J Johnson
    Division of Nephrology, Hypertension, and Renal Transplantation, University of Florida, Gainesville, Florida 32610 0224, USA
    J Hypertens 26:381-91. 2008
    ....
  34. ncbi Diabetic eNOS-knockout mice develop accelerated retinopathy
    Qiuhong Li
    Department of Ophthalmology, College of Medicine, University of Florida, Gainesville, Florida 32610 0284, USA
    Invest Ophthalmol Vis Sci 51:5240-6. 2010
    ..This study was undertaken to determine the role of eNOS in the development of diabetic retinopathy (DR), by investigating the functional consequences of its deficiency in the diabetic state...
  35. ncbi Fructose, but not dextrose, accelerates the progression of chronic kidney disease
    Michael S Gersch
    Division of Nephrology, Dialysis and Transplantation, University of Florida, Gainesville, Florida 32610 0224, USA
    Am J Physiol Renal Physiol 293:F1256-61. 2007
    ..In conclusion, consumption of a high-fructose diet greatly accelerates progression of chronic kidney disease in the rat remnant kidney model...
  36. ncbi Could uric acid have a role in acute renal failure?
    A Ahsan Ejaz
    Division of Nephrology, Hypertension and Transplantation, University of Florida, Gainesville, FL 32610 0224, USA
    Clin J Am Soc Nephrol 2:16-21. 2007
    ..It is suggested that studies are needed to investigate the role of chronic hyperuricemia on renal outcomes after acute tubular injury...
  37. ncbi Uric acid, the metabolic syndrome, and renal disease
    Pietro Cirillo
    Division of Nephrology, Hypertension and Transplantation, Department of Medicine, University of Florida, PO Box 100224, Gainesville, FL 32608, USA
    J Am Soc Nephrol 17:S165-8. 2006
    ..It is proposed that fructose- and purine-rich foods that have in common the raising of uric acid may have a role in the epidemic of metabolic syndrome and renal disease that is occurring throughout the world...
  38. ncbi Lessons from comparative physiology: could uric acid represent a physiologic alarm signal gone awry in western society?
    Richard J Johnson
    Division of Nephrology, Hypertension and Transplantation, University of Florida, Gainesville, FL 32610, USA
    J Comp Physiol B 179:67-76. 2009
    ....
  39. ncbi Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease
    Richard J Johnson
    Division of Nephrology and Department of Medicine, University of Florida, Gainesville, FL, USA
    Am J Clin Nutr 86:899-906. 2007
    ..Finally, we suggest that high intakes of fructose in African Americans may explain their greater predisposition to develop cardiorenal disease, and we provide a list of testable predictions to evaluate this hypothesis...
  40. ncbi Adverse effects of the classic antioxidant uric acid in adipocytes: NADPH oxidase-mediated oxidative/nitrosative stress
    Yuri Y Sautin
    Division of Nephrology, Hypertension, and Transplantation, Dept of Medicine, University of Florida, Gainesville, FL 32610 0224, USA
    Am J Physiol Cell Physiol 293:C584-96. 2007
    ....
  41. ncbi Hypothesis: could excessive fructose intake and uric acid cause type 2 diabetes?
    Richard J Johnson
    Division of Nephrology, Hypertension and Transplantation, University of Florida, P O Box 100224, Gainesville, Florida 32620 0224, USA
    Endocr Rev 30:96-116. 2009
    ..If diabetes might result from excessive intake of fructose, then simple public health measures could have a major impact on improving the overall health of our populace...
  42. ncbi Subtle renal injury is likely a common mechanism for salt-sensitive essential hypertension
    Richard J Johnson
    Division of Nephrology, Hypertension, and Transplantation, University of Florida, P.O. Box 100224, Gainesville, FL 32610, USA
    Hypertension 45:326-30. 2005
  43. ncbi Thiazide-induced subtle renal injury not observed in states of equivalent hypokalemia
    S Reungjui
    Division of Nephrology, Hypertension and Transplantation, Department of Medicine, University of Florida College of Medicine, Gainesville, Florida, USA
    Kidney Int 72:1483-92. 2007
    ..We also found impaired endothelium-dependent vasorelaxation was linked to mild hypokalemia...
  44. ncbi Role of JAK/STAT pathway in IL-6-induced activation of vascular smooth muscle cells
    Susumu Watanabe
    Baylor College of Medicine, Houston, Tex, USA
    Am J Nephrol 24:387-92. 2004
    ..We hypothesized that this stimulation occurs via the JAK (janus-activated kinase)/STAT (signal and transducers and activators of transcription) signaling pathway...
  45. ncbi Hyperuricemia induces endothelial dysfunction
    Uday M Khosla
    Baylor College of Medicine, Department of Medicine, Division of Nephrology, Houston, Texas 77030, USA
    Kidney Int 67:1739-42. 2005
    ..Therefore, we hypothesized that uric acid induces endothelial dysfunction by inhibiting nitric oxide production...
  46. ncbi Fructose induces the inflammatory molecule ICAM-1 in endothelial cells
    Olena Glushakova
    Division of Nephrology, Hypertension and Transplantation, University of Florida, P O Box 100224, Gainesville, FL 32610 0224, USA
    J Am Soc Nephrol 19:1712-20. 2008
    ..These data suggest that fructose induces inflammatory changes in vascular cells at physiologic concentrations...
  47. ncbi Uric acid and hypertension
    Daniel I Feig
    Department of Pediatrics, Renal Section, MC3 2482, Baylor College of Medicine, 1102 Bates Street, Houston, TX 77030, USA
    Curr Hypertens Rep 8:111-5. 2006
    ..Ongoing clinical trials will elucidate the role of uric acid in human hypertension and will determine whether control of uric acid may be a new way to prevent or treat essential hypertension...
  48. ncbi Reduced expression and impaired kinase activity of a Chk2 mutant identified in human lung cancer
    S Matsuoka
    Howard Hughes Medical Institute, Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, Texas 77030, USA
    Cancer Res 61:5362-5. 2001
    ....
  49. ncbi Tubulointerstitial disease: role of ischemia and microvascular disease
    Takahiko Nakagawa
    Division of Nephrology, Baylor College of Medicine, Houston, Texas 77030, USA
    Curr Opin Nephrol Hypertens 12:233-41. 2003
    ..Here we summarize recent studies on the pathogenesis and consequences of tubulointerstitial disease, emphasizing the role of ischemia and the microvasculature...
  50. ncbi Carbon monoxide and nitric oxide mediate cytoskeletal reorganization in microvascular cells via vasodilator-stimulated phosphoprotein phosphorylation: evidence for blunted responsiveness in diabetes
    Sergio Li Calzi
    Department of Pharmacology and Therapeutics, University of Florida, Gainesville, Florida, USA
    Diabetes 57:2488-94. 2008
    ....
  51. ncbi Hyperuricemia causes glomerular hypertrophy in the rat
    Takahiko Nakagawa
    Department of Medicine Nephrology, Baylor College of Medicine, Houston, Tex 77030, USA
    Am J Nephrol 23:2-7. 2003
    ..Am J Physiol 2002;6:F991-F997]. We hypothesized that hyperuricemia might also induce glomerular changes...
  52. ncbi Endothelial von Willebrand factor release due to eNOS deficiency predisposes to thrombotic microangiopathy in mouse aging kidney
    Takahiro Nakayama
    Division of Nephrology, University of Florida, Gainesville, Florida, USA
    Am J Pathol 176:2198-208. 2010
    ..A lack of nitric oxide likely contributed to the release of vWF, leading to thrombus formation in this model...
  53. ncbi Hypothesis: Uric acid, nephron number, and the pathogenesis of essential hypertension
    Daniel I Feig
    Renal Section, Department of Pediatrics, Baylor College of Medicine, Houston, Texas, USA
    Kidney Int 66:281-7. 2004
    ..Genetic, physiologic, and epidemiologic studies provide clues to its origins, but a clear understanding has been elusive. Recent experimental and clinical studies have implicated uric acid in the onset of essential hypertension...
  54. ncbi Mild hyperuricemia induces glomerular hypertension in normal rats
    Laura G Sanchez-Lozada
    Department of Nephrology, Instituto Nacional de Cardiologia I Chavez, 14080 Mexico City, Mexico
    Am J Physiol Renal Physiol 283:F1105-10. 2002
    ..Glomerular hypertension may be partially mediated by an abnormal vascular response to systemic hypertension due to arteriolopathy of the afferent arteriole...
  55. ncbi Activation of Src kinase in platelet-derived growth factor-B-dependent tubular regeneration after acute ischemic renal injury
    Mikiko Takikita-Suzuki
    Department of Medicine, Shiga University of Medical Science, Seta, Otsu, Japan
    Am J Pathol 163:277-86. 2003
    ..These findings suggest that active Src participates in PDGF-B-dependent regeneration of tubular cells from acute ischemic injury...
  56. ncbi Uric acid, endothelial dysfunction and pre-eclampsia: searching for a pathogenetic link
    Duk Hee Kang
    Division of Nephrology, Ewha Women s University College of Medicine, Seoul, Korea
    J Hypertens 22:229-35. 2004
    ....
  57. ncbi Effects of acute and chronic L-arginine treatment in experimental hyperuricemia
    Laura G Sanchez-Lozada
    Dept of Nephrology, Instituto Nacional de Cardiologia Ignacio Chavez, Juan Badiano 1 14080, Mexico City, Mexico
    Am J Physiol Renal Physiol 292:F1238-44. 2007
    ..On the other hand, chronic l-Arg preserved arteriolar structures probably mediated by the antiproliferative effect of NO on vascular smooth muscle cells...
  58. ncbi Effects of febuxostat on metabolic and renal alterations in rats with fructose-induced metabolic syndrome
    Laura G Sanchez-Lozada
    Dept of Nephrology, Instituto Nacional de Cardiologia Ignacio Chavez, Juan Badiano 1, 14080 Mexico City, Mexico
    Am J Physiol Renal Physiol 294:F710-8. 2008
    ..These results provide further evidence for a pathogenic role of hyperuricemia in fructose-mediated metabolic syndrome...
  59. ncbi Fructose-induced metabolic syndrome is associated with glomerular hypertension and renal microvascular damage in rats
    Laura G Sanchez-Lozada
    Dept of Nephrology, Instituto Nacional de Cardiologia Ignacio Chavez, Juan Badiano 1 14080, Mexico City, Mexico
    Am J Physiol Renal Physiol 292:F423-9. 2007
    ..These changes are best observed in rats administered high doses (60% diet) of fructose...
  60. ncbi Uric acid and chronic renal disease: possible implication of hyperuricemia on progression of renal disease
    Duk Hee Kang
    Division of Nephrology, Ewha Women s University College of Medicine, Seoul 110 126, Korea
    Semin Nephrol 25:43-9. 2005
    ....
  61. ncbi Nephron number, uric acid, and renal microvascular disease in the pathogenesis of essential hypertension
    Daniel I Feig
    Hypertension 48:25-6. 2006
  62. ncbi Hypokalemic nephropathy is associated with impaired angiogenesis
    Sirirat Reungjui
    Division of Nephrology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand
    J Am Soc Nephrol 19:125-34. 2008
    ..In conclusion, hypokalemic nephropathy is associated with impaired renal angiogenesis, evidenced by progressive capillary loss, reduced endothelial cell proliferation, and loss of VEGF expression...
  63. ncbi Overexpression of calmodulin in pancreatic beta cells induces diabetic nephropathy
    Yukio Yuzawa
    Department of Nephrology, Nagoya University Graduate School of Medicine, 65 Tsuruma cho, Showa Ku, Nagoya 466 8550, Japan
    J Am Soc Nephrol 19:1701-11. 2008
    ..This model may prove useful in the study of the pathogenesis and treatment of DN...
  64. ncbi Uric acid causes vascular smooth muscle cell proliferation by entering cells via a functional urate transporter
    Duk-Hee Kang
    Division of Nephrology, Ewha Women's University College of Medicine, Seoul, Korea
    Am J Nephrol 25:425-33. 2005
    ..The specific transporter(s) responsible for the urate uptake remains to be determined...
  65. ncbi Microarray and bioinformatic detection of novel and established genes expressed in experimental anti-Thy1 nephritis
    Denise M Sadlier
    Department of Medicine and Therapeutics, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Ireland
    Kidney Int 68:2542-61. 2005
    ..Administration of anti-Thy1 antibody results in phases of acute mesangial injury (day 2), cell proliferation (day 5), matrix expansion (days 5 and 7), and subsequent healing (day 14)...